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EPHB2 — GSK3B

Text-mined interactions from Literome

Mai et al., J Neurochem 2002 (Neuroblastoma) : Overexpression of GSK3beta did not affect BDNF induced phosphorylation of Akt, ERK1/2 , or FKHRL1, but abolished CREB phosphorylation induced by BDNF
Hetman et al., J Biol Chem 2002 : Here, we report that inhibition of ERK1/2 increased the basal activity of GSK3beta in cortical neurons and that both ERK1/2 and PI3K were required for brain derived neurotrophic factor (BDNF) suppression of GSK3beta activity ... Although both PI3K and ERK1/2 inhibited GSK3beta activity, neither had an effect on GSK3beta phosphorylation at Tyr-216
Goodenough et al., Brain Res 2004 (Neurotoxicity Syndromes) : Indeed, GSK-3beta phosphorylation occurred in response to kainic acid exclusively in the affected hippocampus, but not as a consequence of ERK activation
Wong et al., Life Sci 2005 (Enterovirus Infections) : The activity of GSK3beta , a downstream target of these pathways, was negatively regulated by the activation of both MAPK/ERK and PI3K/Akt
Almeida et al., J Biol Chem 2005 : Wnt3a induced phosphorylation of GSK-3beta and downstream activation of beta-catenin mediated transcription required ERK , PI3K, and Akt signaling
Perez-Pinera et al., Mol Cell Biochem 2006 (Neoplasm Invasiveness...) : This response was both time- and dose dependent, it was independent of the Akt signaling pathway and did not increase steady state levels of phosphorylation of beta-catenin, although the data suggested that activated GSK3beta could regulate the activity of ERK1/2
Neary et al., J Neurosci Res 2006 : PKC also links P2 receptors to ERK in astrocytes, but inhibition of ERK signaling did not block phosphorylation of Ser9-GSK3beta stimulated by P2 receptors
Naska et al., J Neurosci 2006 : Specifically, inhibition of GSK-3beta led to increased ERK phosphorylation, and inhibition of MEK completely blocked the effects of GSK-3beta inhibition on dendrite initiation and growth
Xu et al., J Cell Biochem 2008 (MAP Kinase Signaling System) : The activation of ERK1/2 was inhibited by a PI3K inhibitor, LY294002, but U0126, a ERK1/2 inhibitor did not inhibit phosphorylation of Akt and GSK3 beta
Kim et al., Brain Res 2007 : In this study, we investigated whether GSK-3beta inhibition is involved in ERK activation, which affects the activation of NF-kappaB and induction of MMP-9 in cultured rat primary astrocytes ... Pretreatment of U-0126 ( MEK1/2 inhibitor ) completely abolished the GSK-3beta inhibition induced phosphorylation of ERK1/2 ... These data suggest that GSK-3beta inhibition mediates ERK1/2 activation followed by NF-kappaB activation, which directly regulates the induction of MMP-9 in rat primary astrocytes
Caraci et al., Pharmacol Res 2008 : This study demonstrates that TGF-beta1 induces alpha-SMA expression and collagen production in human lung fibroblasts via ERK1/2 activation, GSK-3beta inhibition and nuclear beta-catenin translocation
Mariappan et al., J Biol Chem 2008 (Diabetes Mellitus, Type 2...) : Incubation with selective kinase inhibitors showed that high glucose- and high insulin induced laminin beta1 synthesis and phosphorylation of GSK3beta were dependent on PI 3-kinase, Erk , and mTOR
Nemoto et al., J Pharmacol Sci 2009 : In cultured bovine adrenal chromaffin cells, 1 ) constitutive and negatively regulated activities of GSK-3beta up- and down-regulated insulin receptor, insulin receptor substrate-1 (IRS-1), IRS-2, and Akt levels via controlling proteasomal degradation and protein synthesis ; 2 ) nicotinic receptor/protein kinase C-alpha (PKC-alpha)/extracellular signal regulated kinase ( ERK ) pathway up-regulated IRS-1 and IRS-2 levels, enhancing insulin induced the phosphoinositide 3-kinase (PI3K)/Akt/GSK-3beta pathway ; 3 ) inhibition of calcineurin by cyclosporin A or FK506 down-regulated IRS-2 level, attenuating insulin-like growth factor-I (IGF-I) induced ERK and GSK-3beta pathways ; and 4 ) insulin, IGF-I or therapeutics ( e.g., lithium ) up-regulated the voltage dependent Na(v)1.7 sodium channel